Osmotin Protects H9c2 Cells from Simulated Ischemia-Reperfusion Injury through AdipoR1/PI3K/AKT Signaling Pathway
Open accessAbstract
Objective: This study aimed to investigate the effect of osmotin on myocardial ischemia/reperfusion (I/R), as well as the underlying mechanisms. Methods: In vitro I/R injury model was established on rat cardiac myoblast H9c2 cells by oxygen and glucose deprivation followed by reperfusion (OGD/R). Cells were administrated with osmotin, and transfected with small interfering RNAs (siRNAs) which specifically target adiponectin receptor 1 or 2 (AdipoR1/2). Besides, the cells were incubated with or without LY294002 as inhibitor of phosphatidylinositol 3-kinase (PI3K) under OGD/R condition. Cell viability, apoptosis, expressions of apoptosis-related proteins and inflammatory factors were analyzed. Results: The results showed that osmotin significantly increased H9c2 cells viability compared with the cells treated with vehicle (P < 0.05), and decreased H9c2 cells apoptosis by regulating expressions of apoptosis-related proteins. Moreover, we observed that osmotin statistically reduced the release of proinflammatory factors and increased the release of anti-inflammatory factors in H9c2 cells (P < 0.05). However, these effects were markedly reversed by AdipoR1 silence but not AdipoR2. Furthermore, osmotin dramatically upregulated the phosphorylation levels of PI3K, AKT, ERK, and downregulated the phosphorylation level of NF-κB (P < 0.05). While administration of LY294002 reduced cell viability, increased cell apoptosis, and aggravated inflammatory response (P < 0.05). Conclusion: Our results suggested that the protective effect of osmotin on the simulated OGD/R injured H9c2 cells might be associated with AdipoR1/PI3K/AKT signaling pathway.
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Osmotin has potential effects for counteracting obesity, diabetes and cardiovascular diseases.
“Several in vitro and in vivo studies revealed its potential effects for counteracting obesity, diabetes and cardiovascular diseases [125,126,127].”
From Adiponectin and Its Mimics on Skeletal Muscle: Insulin Sensitizers, Fat Burners, Exercise Mimickers, Muscling Pills … or Everything Together? (2020) · cites this paper as [126]
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- Authors
- Liu, J., Sui, H., Zhao, J., & Wang, Y.
- Affiliations
- Xinxiang Central Hospital (CN)
- Corresponding author
- Wang, Yan
- Venue
- Frontiers in Physiology
- Publisher
- Frontiers Media SA
- Published
- 2017-09-25
- Volume
- 8
- Pages
- 611-611
- ISSN
- 1664-042X (ISSN-L)
- PMC
- PMC5622187
- OpenAlex
- W2760757733
- Cited by
- 38
- References
- 48
- Citations by year
- 2025: 2 · 2024: 3 · 2023: 2 · 2022: 3 · 2021: 6 · 2020: 11 · 2019: 5 · 2018: 6
- FWCI
- 4.72
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by
- Locations
- Frontiers in Physiology (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Topics
- Health Sciences › Medicine › Pathology and Forensic Medicine › Cardiac Ischemia and Reperfusion
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Keywords
- osmotin, myocardial ischemia-reperfusion injury, AdipoR1, AdipoR2, PI3K/Akt signaling, cardioprotection, apoptosis, inflammation, NF-κB, ERK, oxygen-glucose deprivation/reoxygenation, H9c2 cells, cardiomyocytes
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